Brain Research最新文献

{"title":"Ghrelin-based interventions in preclinical models of Parkinson’s disease: a systematic review","authors":"Henrique José Cavalcanti Bezerra Gouveia ,&nbsp;Osmar Henrique dos Santos-Júnior ,&nbsp;Johannes Frasnelli ,&nbsp;Alexandre Fisette ,&nbsp;Joaci Pereira dos Santos Júnior ,&nbsp;Marcos Antônio da Silva Araújo ,&nbsp;Eulália Rebeca da Silva-Araújo ,&nbsp;Ana Elisa Toscano ,&nbsp;Raul Manhães de Castro","doi":"10.1016/j.brainres.2026.150187","DOIUrl":"10.1016/j.brainres.2026.150187","url":null,"abstract":"<div><div>Ghrelin plays a crucial role in metabolism and gastrointestinal function. In the central nervous system, ghrelin modulates both hedonic and homeostatic control of eating behavior. Ghrelin promotes neuron survival by reducing apoptosis, inflammation, and oxidative stress, making it a potential therapeutic agent for neurodegenerative diseases. Parkinson’s Disease (PD) is a neurodegenerative disease characterized by motor and non-motor symptoms. The motor impairments result primarily from the progressive degeneration of dopaminergic neurons in the substantia nigra pars compacta. Individuals with PD exhibit reduced levels of fasting and postprandial plasma ghrelin, and its receptors (GHSR) are expressed in the substantia nigra. Thus, this review aimed to evaluate the effects of ghrelin or GHSR agonists administration in experimental models of PD. A systematic search was conducted across PubMed, Scopus, Web of Science, and Embase. The 12 included studies involved PD models induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), 6-hydroxydopamine (6-OHDA), as well as A53T transgenic mice. Interventions were performed with acylated and/or des-acylated ghrelin, in addition to the GHSR agonist HM01. Intervention with ghrelin was able to reduce dopaminergic neurodegeneration and improve motor function, while also positively impacting metabolic and gastrointestinal functions, expanding its relevance to non-motor consequences of PD. Considering that most results were obtained using acute toxin-induced models and only male animals, further studies using progressive PD models and evaluating sex differences are needed. Thus, although preclinical evidence supports ghrelin or GHSR agonists as promising agents for treatment, future studies will be essential to inform clinical translation and optimize therapeutic strategies for individuals with PD.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1876 ","pages":"Article 150187"},"PeriodicalIF":2.6,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146123847","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Alpha suppression during non-painful tactile stimulation","authors":"Çağdaş Güdücü ,&nbsp;Güliz Akın Öztürk ,&nbsp;Zehra Ülgen","doi":"10.1016/j.brainres.2026.150191","DOIUrl":"10.1016/j.brainres.2026.150191","url":null,"abstract":"<div><div>Alpha-band power is considered as a marker of sensory processing–related cortical states, including sensory suppression and the temporal organization of sensory input. This study aimed to investigate whether alpha-band power of electrophysiological brain responses is modulated by different interstimulus intervals during repetitive, non-painful tactile stimulation. Non-painful tactile stimuli were delivered to the index finger of the right hand with different interstimulus intervals (ISI) of 2 s (s), 4 s, and 8 s via a pneumatic stimulator. A separate session was conducted for each ISI in a pseudorandomized order. The electroencephalogram was recorded in all sessions with 24 volunteers. The results of the analysis showed that the alpha activity was lowest at ISI₄ and highest at ISI₈. This pattern was consistently observed in both the central and parietal regions. In the ISI₂ session, although no notable variation among the frontal, central, and parietal areas was observed, the most pronounced activity was observed in the frontal region in the ISI₄ session. The highest level of alpha activity was observed in the central area during the ISI₈ session. Variations in interstimulus intervals affect inhibitory control and sensory processing in the brain. The frontal cortex appears to manage attention and cognitive control more efficiently at intermediate intervals (ISI₄), whereas the central region shows greater involvement in processing tactile inputs at longer intervals (ISI₈).</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1876 ","pages":"Article 150191"},"PeriodicalIF":2.6,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146137031","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of the dentate gyrus of hippocampus on acute pain modulation: Investigating of dopaminergic-opioidergic interactions in pain-related behaviors in the tail-flick test","authors":"Sahar Sadeghzadeh Sotoudeh ,&nbsp;Shima Abtin ,&nbsp;Roghayeh Mozafari ,&nbsp;Abbas Haghparast","doi":"10.1016/j.brainres.2026.150155","DOIUrl":"10.1016/j.brainres.2026.150155","url":null,"abstract":"<div><div>Previous studies have shown that injections of opioid and dopamine agonists alone into the dentate gyrus (DG) increase the threshold for acute pain responses. Therefore, this study aimed to investigate whether the opioid and D1-like dopamine receptor (D1R) interact to modulate acute pain in DG. One hundred and forty-seven adult male Wistar rats were cannulated unilaterally in the DG. Separate groups of animals received different doses of SCH23390 (6, 12, and 24 mmol/0.5 μL), a D1R antagonist, before injection of an effective dose of morphine (25 mmol/0.5 μL). In another experiment, animals received different naloxone (5, 15, and 45 mmol/0.5 μL) dose, an opioid receptor antagonist, before administering the effective dose of SKF38393 (6 mmol/0.5 μL). Acute pain threshold was assessed using the tail-flick test. Behavioral data analysis indicated that blockade of D1R in the DG significantly attenuated morphine-induced antinociception (P &lt; 0.001). Furthermore, the antinociceptive effects of SKF38393 were significantly reduced by blocking opioid receptors in the DG (P &lt; 0.01). Interestingly, the effect of SCH23390 in reducing the antinociceptive effects of morphine (η2 = 0.65) was numerically higher than the effect of naloxone in reducing the antinociceptive effects of SKF38393 (η2 = 0.46). The results suggest a strong interaction between opioidergic and dopaminergic systems in the DG in modulating acute pain. These findings can be used to reveal the precise mechanisms of pain modulation in brain circuits and to develop new strategies in pain management with greater efficacy and fewer side effects.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1875 ","pages":"Article 150155"},"PeriodicalIF":2.6,"publicationDate":"2026-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145942368","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluation of neurobiochemical and behavioral responses to carvone nanoemulsion: A neuroprotective approach for Alzheimer’s disease-associated dementia in a rat model","authors":"Sahand Kabiri ,&nbsp;Pariya Gholizadeh Dangheralou ,&nbsp;Farnaz Khazaeifard ,&nbsp;Samir Rostami Mehr ,&nbsp;Seyedeh Mohadeseh Mansouri ,&nbsp;Nahal Rahimi Rad ,&nbsp;Saeid Abbasi-Maleki","doi":"10.1016/j.brainres.2026.150143","DOIUrl":"10.1016/j.brainres.2026.150143","url":null,"abstract":"<div><h3>Background</h3><div>Antioxidant supplements have emerged as promising strategies to mitigate the impact of Alzheimer’s disease (AD) and associated dementia. We explored the neuroprotective potential of Carvone nanoemulsion (CANO) using a rat model of AD-associated dementia.</div></div><div><h3>Method</h3><div>Our experimental groups comprised non-AD control rats (CON), untreated AD rats (AD), and AD rats treated with CANO at two different dosages: 40 mg/kg (CANO40) and 80 mg/kg (CANO80). We assessed various behavioral parameters, malondialdehyde (MDA) and brain-derived neurotrophic factor (BDNF) levels,<!--> <!-->ferric-reducing ability of plasma (FRAP).</div></div><div><h3>Results</h3><div>AD induction caused a significant reduction in step-through latency (P &lt; 0.001), center time (P &lt; 0.001), the number of visits (P &lt; 0.001), and total distance traveled (P &lt; 0.001), time spent in open arms (P &lt; 0.001), and both FRAP (P &lt; 0.001) and BDNF levels (P &lt; 0.001) in comparison to the CON group, while elevating escape latency, time in target zone and platform location latency, and MDA levels (P &lt; 0.001). Treatment with CANO, particularly at the CANO80 dosage, significantly improved these parameters compared to the AD group, resulting in decreased time in the target zone (P &lt; 0.001), escape latency (P &lt; 0.001), and platform location latency (P &lt; 0.001) and higher FRAP (P &lt; 0.05) and BDNF levels (P &lt; 0.05), along with decreased MDA levels (P &lt; 0.05).</div></div><div><h3>Conclusion</h3><div>CANO, especially at the 80 mg/kg dosage, shows promise in alleviating symptoms associated with AD-associated dementia. However, further research is warranted to validate and expand upon these findings.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1875 ","pages":"Article 150143"},"PeriodicalIF":2.6,"publicationDate":"2026-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145899448","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Covert attention modulates visual perception in early infancy","authors":"Shuma Tsurumi ,&nbsp;So Kanazawa ,&nbsp;Masami K. Yamaguchi ,&nbsp;Jun-ichiro Kawahara","doi":"10.1016/j.brainres.2026.150186","DOIUrl":"10.1016/j.brainres.2026.150186","url":null,"abstract":"<div><div>Visual attention enhances perception by facilitating detection, localization, and identification of stimuli. Classic accounts propose that such modulation depends on feedback from higher cortical areas, whereas recent evidence suggests contributions from feedforward processes within early visual regions. Infants provide a unique opportunity to test these mechanisms because their feedback pathways remain immature during the first half of the first year. Here, we examined whether covert attention influences perception in 3- to 4-month-old infants using a spatial cueing task. In Experiment 1, infants discriminated orientation, and in Experiment 2, they discriminated motion direction of cued peripheral gratings, despite not making eye movements. These findings demonstrate that covert attention modulates perception in early infancy, indicating that attentional effects can emerge via feedforward processes before the maturation of top–down feedback.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1875 ","pages":"Article 150186"},"PeriodicalIF":2.6,"publicationDate":"2026-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146075108","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Programmed cell death pathways in Parkinson’s disease: Spotlight on ferroptosis and pyroptosis","authors":"Veerta Sharma,&nbsp;Reet Verma,&nbsp;Prateek Sharma,&nbsp;Thakur Gurjeet Singh","doi":"10.1016/j.brainres.2026.150165","DOIUrl":"10.1016/j.brainres.2026.150165","url":null,"abstract":"<div><div>Parkinson’s disease (PD) characterized by the selective loss of dopaminergic neurons in the brain resulting in motor and cognitive deficits. While apoptosis has long been considered a primary mechanism of neuronal death in PD, emerging evidence highlights the significant roles of non-apoptotic programmed cell death pathways, particularly ferroptosis and pyroptosis-in driving PD progression. Ferroptosis is form of cell death that is dependent on iron and driven by lipid peroxidation, appears to be associated with PD. On the other hand, Pyroptosis, a caspase-1-dependent inflammatory cell death pathway mediated by activation of inflammasome and release of pro-inflammatory cytokines such as interleukin-1β (IL-1β) and IL-18. Both pathways contribute to the neurodegeneration in PD through distinct yet interconnected pathways. Therefore, this review highlights molecular mechanisms underlying ferroptosis and pyroptosis in PD and recent advances in pharmacological strategies targeting these pathways.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1875 ","pages":"Article 150165"},"PeriodicalIF":2.6,"publicationDate":"2026-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145965149","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RhoA regulates morphine associated NMDA receptor signaling in the prelimbic region of medial prefrontal cortex pyramidal neurons","authors":"Qiufeng Dong ,&nbsp;Xin Wang ,&nbsp;Yuqi Wen ,&nbsp;Jian Fu ,&nbsp;Liangjun Zhang ,&nbsp;Yile Zhang ,&nbsp;Zhiqiang Yan ,&nbsp;Liang Qu","doi":"10.1016/j.brainres.2026.150184","DOIUrl":"10.1016/j.brainres.2026.150184","url":null,"abstract":"<div><div>Opioid dependence (OD) involves maladaptive neuroplasticity in brain reward circuits, particularly within the medial prefrontal cortex (mPFC). While RhoA and NMDA receptors (NMDARs) are implicated in addiction-related synaptic plasticity, their specific interaction within mPFC subregions remains unclear. Using male Sprague-Dawley rats (6 weeks old), we investigated the role of RhoA signaling in the prelimbic cortex (PLC) via behavioral, molecular biological, and electrophysiological assays. Intra-PLC infusion of the RhoA inhibitor Rhosin significantly attenuated morphine-induced conditioned place preference and locomotor sensitization. Furthermore, repeated morphine administration (RMA) upregulated RhoA expression in layer 5 pyramidal neurons. In vitro whole-cell patch-clamp recordings of layer 5 neurons, stimulated at layer 2/3, revealed that Rhosin reduced the amplitude of synaptic NMDAR-mediated excitatory postsynaptic currents. Additionally, using an activity-dependent MK-801 block to isolate extrasynaptic components, we demonstrated that RhoA inhibition significantly attenuated extrasynaptic NMDAR activation, likely by limiting glutamate spillover during high-frequency stimulation. These findings elucidate a critical mechanism by which RhoA mediates opioid-induced neuroadaptations through the regulation of both synaptic and extrasynaptic NMDAR activity, identifying RhoA in the PLC as a promising therapeutic target for opioid dependence.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1875 ","pages":"Article 150184"},"PeriodicalIF":2.6,"publicationDate":"2026-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146075106","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Single administration of vitamin C produces rapid antidepressant-like effects in female mice: A possible role of dopamine D2 receptor signalling","authors":"Ming-Lian Luo ,&nbsp;Yi-Heng Li ,&nbsp;Xue-Mei Gao ,&nbsp;Yuan-Jian Yang ,&nbsp;Shu-Zhen Jiang","doi":"10.1016/j.brainres.2026.150181","DOIUrl":"10.1016/j.brainres.2026.150181","url":null,"abstract":"<div><h3>Background</h3><div>The lifetime prevalence of depression is significantly higher in women. But the lack of ideal antidepressant severely limits therapies for female specific depressive disorders like perinatal depression. Herein, we evaluated whether vitamin C (ascorbic acid), a widely used nutritional supplement and perinatal therapeutic agent, could serve as a potential treatment for female-related depressive disorders using a chronic restraint stress (CRS) mouse model.</div></div><div><h3>Methods</h3><div>C57BL/6 adult female mice were submitted to a 14-day CRS paradigm to induce depression-like behaviors. The antidepressant potential of vitamin C (200 mg/kg, i.p., a single dose) were assessed in CRS-exposed female mice that exhibited depression-like phenotype. Furthermore, we explored the underlying mechanisms through RNA sequencing, western blotting, and pharmacological interventions.</div></div><div><h3>Results</h3><div>Vitamin C rapidly ameliorated depression-like phenotypes in CRS-exposed female mice within 24 h. The sucrose preference test indicated that the antidepressant effect of vitamin C lasted for more than 72 h. Transcriptome sequencing analysis revealed that vitamin C reversed CRS-induced transcriptional alterations in 104 genes in the medial prefrontal cortex (mPFC) of female mice, including the dopamine receptor D2 (D2R). Western blotting confirmed that CRS suppressed the D2R-ERK1/2-CREB-BDNF pathway in the mPFC, which was effectively rescued by vitamin C. The antidepressant effect of vitamin C was antagonized by the D2R antagonist sulpiride. Additionally, protein–protein interaction network analysis revealed functional linkages between D2R and other vitamin C-regulated stress-sensitive genes.</div></div><div><h3>Conclusions</h3><div>Our findings suggest that vitamin C may serve as an ideal candidate for the treatment of depression in females, potentially through the restoration of the D2R-BDNF pathway.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1875 ","pages":"Article 150181"},"PeriodicalIF":2.6,"publicationDate":"2026-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146036610","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"From truth to deception: a network control theory perspective on brain connectivity and cognitive dynamics","authors":"Ali Rahimi Saryazdi ,&nbsp;Farnaz Ghassemi ,&nbsp;Fatemeh Parastesh ,&nbsp;Karthikeyan Rajagopal ,&nbsp;Sajad Jafari","doi":"10.1016/j.brainres.2026.150159","DOIUrl":"10.1016/j.brainres.2026.150159","url":null,"abstract":"<div><div>Deception represents a sophisticated mental activity that modifies the brain’s dynamic operations. Understanding how brain activity changes during deceptive behavior is important for both cognitive neuroscience and practical applications such as lie detection. Recently, network control theory (NCT) has emerged as a novel tool that combines principles from network science and control theory, offering a powerful framework for quantifying how easily the brain can transition between different cognitive states. In this study, NCT is applied for the first time to examine the effects of deception on brain functional connectivity (FC). Electroencephalogram signals are recorded from 22 participants during a visual task designed to elicit deception. The phase lag index method is then employed to construct FC networks for both truthful and deceptive conditions. The brain is modeled as a linear dynamical system, and two control metrics, average controllability and modal controllability, are computed across five frequency bands: delta, theta, alpha, beta, and gamma. The results reveal significant differences in brain dynamics between the two conditions. In the delta and beta bands, average controllability is significantly higher during truthful responses (p-value &lt; 0.005), while in the gamma band, it is elevated during deception. Additionally, in the beta and gamma bands, modal controllability is significantly higher during deceptive responses (p-value &lt; 0.005). It is observed that during deception, the control energy spectrum shifts from predominance in lower frequencies, which is more evident in truthful responses, toward higher frequencies where energy increases during deception. The outcomes imply that brain connectivity patterns are affected by deceptive behavior and highlight the potential of NCT in advancing deception-related investigations.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1875 ","pages":"Article 150159"},"PeriodicalIF":2.6,"publicationDate":"2026-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145951490","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetics of Autism Spectrum Disorder underscores the role of altered spontaneous neuronal activity as a catalyst for the neurodevelopmental anomalies","authors":"Sarani Dey,&nbsp;Abhijit Das","doi":"10.1016/j.brainres.2026.150164","DOIUrl":"10.1016/j.brainres.2026.150164","url":null,"abstract":"<div><div>Autism Spectrum Disorder (ASD) represents a diverse set of neurodevelopmental disorders diagnosed in children exhibiting common behavioral impairments in social communication and excessive repetitive behaviors. Genetic approaches and large-scale genomic studies have uncovered hundreds of ASD-associated genes with diverse molecular functions contributing to various biochemical and physiological pathways. Despite the underlying genetic diversity, the convergence of phenotypic features suggests the disruption in shared neurobiological mechanisms contributing to ASD. Spontaneous neuronal activity (SNA), the stimulus-independent firing of neurons, which is observed even during neuronal development, has been known to be crucial for neural circuit maturation. Functional neuroimaging studies have demonstrated that SNA is a central process disrupted in ASD patients and mutation-based animal and cellular models. SNA orchestrates critical developmental programs during neuronal maturation such as dendritic arborization, synaptic pruning, excitatory-inhibitory balance, and activity-dependent transcriptional regulation. Perturbations in these dynamics may provide a unifying mechanistic framework linking genetic mutations to abnormal circuit formation and behavioral anomalies. In this review, we collate the genetic and genomic studies to evaluate the contribution of ASD genes in regulating the spontaneous firing of neurons. We classify ASD genes into generators, sensors, transducers, and responders of activity-induced signals and discuss their roles in regulating membrane excitability, transducing the signal to cytoplasmic or nuclear targets to transform the neuronal gene expression program, eventually impacting neuronal and synaptic development. We attempt to substantiate the contribution of altered SNA as the single major common neurological mediator connecting genetic mutations with the common behavioral irregularities manifested in ASD.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1875 ","pages":"Article 150164"},"PeriodicalIF":2.6,"publicationDate":"2026-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145988252","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}